These catfish evolved to survive in warm, humid rivers–where oxygen levels in the water can drop dangerously low at night. So while they breathe through their gills most of the time, the fish also have the option of swimming to the surface and taking a big gulp of air.

Behavioral ecologist Shaun Killen of the University of Glasgow wondered whether something in the social lives of catfish might be driving them to the river surface, so he teamed with catfish researchers at the Federal University of Sāo Carlos in Brazil to find out more.

In the experiment, the scientists assigned the catfish to groups of four per tank and counted the number of air-breaths. They repeated the test at several different dissolved oxygen levels and then compared the group counts to how often the fish air-breathed while alone.

[Above: An African sharptooth catfish that has jumped out of the water at Mlondozi Ford in South Africa. Image by Bernard Dupont via Wikimedia Commons and CC-BY-SA-2.0]

And the culprits behind the behavior were pretty easy to spot.

“There would be a dominant fish in the group that was sort of a jerk and biting all of the other ones and making them air-breathe, and then they [the dominant jerk-fish] would come up and breathe after,” Killen says.

Most isolated catfish go up and breathe air when they need to and only when they need to, Killen says. But when there’s a jerk-fish around, it’s a different story.

There’s no way to read a catfish’s mind, so it’s not clear why exactly the dominant fish nip and nudge the others. However, Killen thinks that it has to do with threats at the river’s surface, such as sharp-eyed birds ready to swoop at the first catfish they see.

“If that dominant fish wants to go up and take a breath, maybe it doesn’t want to be the first one to go up,” Killen says. But perhaps, if the dominant fish can start an air-gulping party by going around biting the other fish, then it will benefit from safety in numbers at the surface.

This potential explanation is not entirely unlike the scene in Raiders of the Lost Ark, where Sallah (John Rhys Davies) and Indiana Jones (Harrison Ford) have opened up an ancient burial chamber, only to find it teeming with snakes. So Sallah looks at Indy and tells him, “Asps. Very dangerous. You go first.”

Killen compares the fish’s behavior to the way humans behave while waiting to cross a busy street. “A lot of times you’ll just follow someone else if they decide to cross the street,” he says. “You think ‘Ok, they’re going. It must be safe for me to go.’ That’s something else we see in social animals, that they kind of rely on others for social information.”

Except instead of just waiting, the “leader” fish may be moving things along by pushing, biting, and nipping at their comrades’ tails.

Then, again, the behavior may not be deliberate on the “bully” fish’ part. And it remains to be seen whether these results from a lab experiment line up with what African sharptooth catfish do in the wild.

Still, Killen thinks that understanding the catfish group dynamic will be important going forward, saying, “It changes their behavior altogether, to where they’re showing behaviors that they would never have done when they were alone.”

tl;dr:

African sharptooth catfish can breathe air (when they want to), but going to the surface is dangerous. So some catfish goad others into breathing first.

Human speaking voices come in a dizzying array of tones. They can be raspy or reedy, lilting or monotone, chirpy or sonorous, nasal or throaty, breathy or booming, and that’s before we even start describing accents.

Most mammals, including humans, use their vocal tracts to make noise, and so slight variations in the anatomies of our voice boxes, throats, mouths, and nasal passages give our voices unique timbres.

Perhaps, not surprisingly, we can use variation in vocal qualities to tell people apart. (Some people have a lot more acuity at this than others, but most of us can recognize our favorite singers, even on songs we haven’t heard before and distinguish our dog’s bark from the neighbors’ dog’s yapping.)

“If you answer the phone, and it’s someone you know very well, you know the voice, and they don’t have to tell you their name,” explains behavioral biologist Laela Sayigh of Hampshire College. “That’s how really every other mammal that has ever been studied identifies each other.”

With one notable exception–dolphins.

Yup, the cleverest animals in the sea seem to be unable to tell each other’s voices apart. Instead, dolphins tell each other apart by listening for “signature whistles,” which function like human names or call-signs.

In a previous study, Sayigh and her colleagues caught wild bottlenose dolphins off the coast of Florida and held them (gently) within a small underwater area while they recorded audio of the dolphins’ whistles, both signature and otherwise.

Later, they caught and held the dolphins again and played the a mixtape. audio recordings of dolphin whistles back to other dolphins. When the dolphins heard recordings of a relative’s (usually a mom or a sibling) signature whistle, the dolphins would turn their heads toward the sound.

The dolphins even turned their heads toward computer-produced versions of their moms and siblings’ signature calls.

But in a new study, Sayigh and her colleagues tried playing recordings of relatives’ “non-signature” whistles and got no reaction. (Other than the usual “let go of me, human!” behavior.)

[Correction: 10/2/17: In an email, Sayigh pointed out to me that there isn’t really a typical dolphin reaction to being held. “The animals are quite different in how they respond,” she wrote. Also, I was obviously projecting the “let go of me, human!” part. We have no way of knowing what the dolphins were thinking.]

In other words, the dolphins were more likely to react to a computer voice saying “Hello. This is Mom.” than Mom’s voice saying something else.

Sayigh says that anatomical differences combined with dolphins’ underwater lifestyle may explain why dolphins don’t seem to recognize their mothers’ and siblings’ voices. Unlike most mammal calls, dolphins whistle through a system of air sacs located around their blowhole, as opposed to calling through their vocal tract.

When dolphins dive down deep, scientists hypothesize that the increased water pressure could change the shape of those sacs, making the timbre of a dolphin’s whistle an unreliable identifier. No one has done studies on dolphin calls at 100 meters below the surface; doing wild dolphin studies in the shallows is already pretty difficult. But Sayigh thinks that “air sacs might slightly deform, changing the tone of whistles” is a pretty safe conjecture.

“There aren’t many contexts in human society that match that, because we don’t live in a three dimensional environment with very limited visual capabilities,” says Sayigh. “But if you just said, ‘I’m here!’ there could be ten other dolphins that that could apply to, but if you say your own name, then there’s not much question about who’s saying that.”

But naming yourself is easier said than done. Coming up with signature sounds requires the ability to imitate and invent new patterns. The vast majority of animals, including most of our closest relatives, communicate through “hardwired” sounds that they can produce at birth.

“If a human infant doesn’t hear another person talking, they’re not going to learn human speech…The language that you hear is what you learn,” explains Sayigh. “But in the case of most non-human mammals, that production side is pretty much hardwired.”

Dolphins, along with birds and humans, are among the tiny minority of animals that learn their calls by listening, imitating, and inventing “signature” sounds. [Correction 10/2/17: Sayigh asked me to clarify: Humans and birds do not invent signature sounds that are directly analogous to signature whistles. Birds and humans do, however, learn to communicate through imitation.] For researchers interested in the evolution of speech and language, that makes dolphins a very important species. And, like humans, dolphins seem to learn new sounds throughout their lives. Identifying the evolutionary pressures that drove dolphins to evolve their learning style might help us understand where the human gift for gab came from.

Sayigh’s study suggests that dolphins may owe their ability to imitate and riff on other sounds not to incredible smarts (although dolphins are very, very smart) or playfulness but rather their inability to tell their friends’ voices apart.

tl;dr:

New research shows that dolphins (probably) can’t tell each other’s voices apart. But that inability may have pushed them to evolve sophisticated vocal learning and to start using signature whistles.

Imagine you’ve been invited to a fancy dinner at a millionaire’s house. The table is set. The silverware gleams. The guests are chitchating about who does what for work and the season finale of Game of Thrones when the dinner host arrives and announces that he has poisoned himself.

The confusion turns to terror when the dinner party host reveals that he has not only poisioned himself but everyone else in the room.

Such a scenario sounds silly, but if you’re a gene in the game of inheritance, “you win or you die.” (Or at least, risk disappearing from the gene pool.) And sometimes the most extremely “selfish genes” are the ones that survive.

Case in point: Some strains of kombucha yeast, the friendly fungus that makes fermented kombucha tea, carry a gene called “wtf4“. (Yes. That is its real, technical name.)

As far as scientists know, wtf4 offers no benefits to its carrier. It doesn’t help kombucha ferment tea leaves or survive refrigeration. It doesn’t boost tendril growth or amp up spore production or even coast along as a neutral passenger. In fact, wtf4 is poisonous to the sex cells (aka “gametes”) of the yeast it lives in. (But not to humans.)

wtf4‘s poisonous nature mainly comes into play during meiosis–the process of typical cells dividing into sex cells with only half the total complement of chromosomes.

Genetics researchers at the Stowers Institute noticed that when yeasts that had just one copy of wtf4 (as opposed to 2 copies) went through meiosis, over 90% of the viable sex cells came out carrying wtf4.

All else being equal, you would expect the sex cells to have a 50-50 chance of inheriting wtf4 from a heterozygous parent. Something was killing off the gametes that didn’t inherit wtf4.

Further investigation revealed that the wtf4 gene was encoding both a poisonous protein…AND the antidote to that poisonous protein.

(For the technically inclined: For a gene to be expressed, it has to have a “transcription start site” where RNA-builder proteins can land and start making an RNA copy of the gene. Gene sequencing revealed that wtf4 actually has two transcription start sites, so the wtf4 can make both a long version and a short version of its protein. The short version is poisonous, but the long version is the antidote…A single gene encoding multiple proteins isn’t strange, but a gene encoding a poison and its own antidote is.)

“Dr. [Sarah] Zanders, our advisor, likens it to a murder mystery party where the host poisons everyone including himself,” says grad student Nicole Nuckolls of the Stowers Institute. “But then the host brings an antidote and saves only himself. That’s a really risky move by this driver, to poison himself and everyone, because if it doesn’t somehow also make the antidote and save itself, it’s dead.”

Nuckolls calls the gene’s behavior “very sneaky but very successful” because its inheritance rate is nearly 100%.

In follow-up experiments, the researchers attached a glowing protein to both WTF4 proteins so that they could see where the WTF4s were turning up in the cell. Much to their surprise, the wtf4-bearing cells released the poison first.

“I thought it was going to be the opposite: you turn on the antidote before you get poison,” says grad student María Bravo Núñez, also of the Stowers Institute. “But it’s just like, ‘No, let’s just kill everyone and hope that I turn on this thing on time and be able to save myself.”

Humans don’t have any genes that correspond to wtf4, but we likely do carry some genes that “cheat” at meiosis–aka “meiotic drivers”–albeit in less dramatic ways. Scientists think that selfish meiotic driver genes may contribute to infertility in humans, a condition that affects 1 in 7 human couples.

Sorting out which gene does what in a genome is a time-consuming process, so spotting parasitic genes–even the extreme examples like wtf4–is difficut, but the researchers hope that understanding wtf4 will make it easier to study meiotic driver genes in humans and eventually address infertility.

“If a couple is struggling with infertility, one of the reasons could be due to selfish genes and genetic conflict,” says Nuckolls. “It’s not because they didn’t do something that was healthy or because they didn’t drink that super-helpful juice that one time...If our work gets even one couple peace-of-mind that their infertility isn’t something they’ve done–it’s just something going on in their biology–then that to me is worth it.”

tl;dr:

A yeast gene called wtf4 cheats at meiosis by encoding both a poison and the antidote to that poison…It’s weird, but understanding its behavior could yield insight into infertility.

The troublemakers weren’t new to the neighborhood. For 300 million years, they had lived in the water column, floating in the sunlight near the surface, sending tiny plumes of toxic gas into the air. That was how they ate: sunlight in, poison out. But it was nothing the ecosystem couldn’t handle. The atmosphere was vast, and the troublemakers were microscopic. The poison diffused. Life went on.

Until something changed. For some reason, there were more green troublemakers. Quadrillions more. So many more that their poison became the air itself. An entire world’s atmosphere transformed. Those that could tolerate the miasma grew and spread. Others survived in pockets of the planet where the new air couldn’t reach them. Uncountable numbers died.

The sunlight-eating oxygen-makers inherited the Earth.

In other words, 2.3 billion years ago, photosynthesis caused a mass extinction.

The great die-off goes by many names: “The Great Oxygenation Event”, “The Oxygen Catastrophe”, “The Oxygen Revolution”, and “The Great Oxidation Event” are just a few. Most biogeochemists who study it just call it The GOE.

“It was the event that allowed large organisms like us to exist, but it was also the largest mass murder in Earth’s history,” explains geochemist Aubrey Zerkle of University of St. Andrew’s in Scotland. “The Great Oxidation Event is essentially the biggest coup that life ever perpetrated on this planet.”

While the sunlight-eaters–known as cyanobacteria or blue-green algae– continued to “pollute” the air with oxygen, other organisms used the deadly gas as fuel. In fact, oxygen gas proved to be the most energy-rich fuel life had ever learned to consume.

The oxygen-breathers grew large, developed complex cell structures, and eventually coalesced into organisms made up of many cells. None of which would have been possible without cyanobacteria and the oxygen they released.

No one knows why the number of blue-green algae exploded 2.3 billion years ago, but the sudden change in atmospheric chemistry left its mark on the rocks that formed at the time. By studying surviving 2.3-billion-year-old rocks, scientists can piece together a rough timeline of the events.

Zerkle and her colleagues were curious about whether nitrogen levels in the rocks could tell them anything new about the post-GOE oceans and their potential for supporting eukaryotic life. Like many elements, nitrogen comes in two versions: Nitrogen-14 (which has 7 neutrons) and Nitrogen-15 (which has 8 neutrons). By looking at the ratio of Nitrogen-14 to Nitrogen-15 in rocks from the GOE and a few million years afterward, her team could estimate which nitrogen-containing chemicals were floating around.

Nitrogen compounds were an essential part of Earth’s biochemistry before the GOE, but the nitrogen-oxygen molecules that modern cells use were rare.

“Nitrogen is fundamental to life,” says Zerkle. “It’s in your DNA, your RNA, [and] all of your proteins have amino groups….Every organism uses it, which means that the availability of nitrogen, even in today’s modern oceans, controls the primary productivity.”

The researchers found evidence that around the time of the GOE, levels of nitrate–a compound with one nitrogen atom and three oxygens bound together–rose in the oceans.”That’s really important from a biological standpoint, because this oxidized nitrogen species is the one that eukaryotes use,” says Zerkle.

“What this does is that it opens up a whole other can of questions,” says Zerkle. “If we know that all this nitrate was available in the environment, there must have been something that was holding these organisms back from evolving.”

The Oxygen Revolution undoubtedly laid the groundwork for the later Eukaryotic Revolution, but the reason behind the timing of these two biological revolutions remains a mystery.

On July 10, 2010, a DC restauranteur came down with what seemed to be food poisoning. He had no energy and no appetite. Rashes flared up. He could barely get out of bed. First hours and then days dragged by without any relief from the symptoms.

The restauranteur’s family sought out doctor after doctor, until finally they were referred to a lab at the NIH (National Institutes of Health) that studies how allergies pass down through families.

His symptoms fit a diagnosis of Mast Cell Activation Syndrome, (MCAS) a disorder where a type of immune cells called mast cells release chemicals that send other immune cells into a destructive frenzy. Ideally, mast cells detect infection and spur other immune cells into action. However, some people’s mast cells have a hair trigger. When mast cells release their chemical contents too often, immune cells end up attacking healthy tissue, causing allergies, stomach issues, and heart palpitations.

[Above: An NIH-produced video about MCAS and Milner’s research into mast cell activation genetics.]

Unfortunately, most treatments for MCAS aim at the symptoms, not the root cause. But the NIH team delved deeper into the genetics and found a pattern: many MCAS-related symptoms run in families.

And oddly enough, hyperflexible joints, dysautonomia, and baby teeth that fail to fall out also ran in many of those families.[Correction 6/15: A commenter has pointed out that “hyperflexible” and “hypermobile” are not interchangeable terms. The term “hypermobile” refers to joints that can move outside the typical range of motion due to laxness in ligaments. “Hypermobility” is also sometimes called “double-jointedness.”] Many of these symptoms skipped generations, only showing up occasionally in individuals, but genetic sequencing revealed the correlation wasn’t coincidence.

In October, NIH scientist Joshua Milner and his team described the genetic disorder in a paper in Nature Genetics. According to the team’s paper, 4-6% of the U.S. population has the genes that predispose them to this syndrome–which has been tentatively named alpha-tryptasemia or “alpha-T”.

The symptoms can be cryptic and unrelenting: Dizziness, chronic pain, irritable bowels, and fainting. For many patients with these conditions, there’s no explanation and no treatment. “These [symptoms] are really all triggers to get an eyeroll from a doctor,” said Milner. But for a sizeable portion of population, these seemingly unrelated problems might be part of the previously undiscovered genetic disorder.

Unknowingly, patients have been struggling to manage this condition for years without being taken seriously by doctors. The symptoms associated with alpha-tryptasemia are what doctors call “nonspecific” or “unspecific,” meaning they could be caused by just about anything.

The symptoms vary quite a bit person-to-person, making it hard to spot. Often, symptoms are mild enough that people just ignore them or don’t think to mention them on the forms they fill out at the doctor’s office. In some cases, the symptoms don’t flare up until a traumatic event in adulthood, Milner says, based on his conversations with patients.

“Patients are almost universally told, ‘It’s all in your head,’ which is awful,” said Milner.

However, the genetic analysis revealed that many people with MCAS, EDS-III, POTS, or other unexplained autoimmune problems have duplicate (or even triplicate) copies of gene that codes for a molecule called alpha-tryptase.

Alpha-tryptase is one of the signalling molecules that mast cells release. Doctors most often test for it when confirming allergic reactions, but tryptase also acts on connnective tissues, mast cells, and blood vessels, Milner says.

“It’s not a marker; it’s the key to ignition,” he added.

Its roles in connective tissue and immune response aren’t the only evidence that alpha-tryptase is the culprit. The gene is located in a stretch of DNA that is particularly prone to copying a section of itself and then pasting the copied DNA back into the chromosome. As a result, some people end up with two or sometimes three copies of the gene on a single chromosome. The study found that people with more copies of the alpha-tryptase gene tended to have more problems.

In the study, the NIH researchers tested patients, their relatives, and about 200 people from the general population. About 1 in 20 people from the general population sample had elevated tryptase, and interviews revealed that many of those people had symptoms such as chronic pain and unexplained gastrointestinal problems. In many cases, the symptoms were so mild that people simply shrugged them off as signs of stress.

(And it’s worth noting that many people with genes for alpha-tryptase don’t seem to have major problems with it. The variability in symptoms and their severity is a big part of why the syndome has gone undescribed for so long.)

About a third of people don’t make alpha-tryptase at all. (There are five other forms of tryptase encoded in the human genome.) Since alpha-tryptase appears to be nonessential, it may be possible to target or counteract it in people whose mast cells make too much.

Treatments for alpha-tryptasemia are still years away.

However, Milner says that just knowing there’s a genetic cause behind their mysterious chronic pains comes as a huge relief to patients. The symptoms of alpha-tryptasemia aren’t life-threatening but they’re chronic, untreatable, disruptive, and frustrating. As the number of symptoms mounts, patients become more overwhelmed, and all the while, doctors keep telling them there’s no explanation and nothing that can be done.

“When you tell people, there’s a genetic disorder behind a lot of this, patients usually start crying when they hear that, because they feel validated,” Milner said.

And now scientists have found evidence that some tumors alter the whole body’s metabolism by “reprogramming” the liver, according to a study in the journal Cell Metabolism. [Full disclosure: I have an accepted an internship position at Cell Press’s media relations office, but I don’t start until January. I conducted the interviews this post is based on prior to accepting the internship.] The consequences of that reprogramming are often deadly.

“The wasting can get so severe in so many patients that it’s estimated to account for 30% of all deaths due to cancer,” explains study co-author Thomas Flint of University of Cambridge. “Lots of people are saying [the cause of death] is the metastasis; it’s this and that, but about 30% of the deaths don’t seem to be directly explained by the tumor.”

Anecdotal accounts often blame chemo for the loss of appetite, but cachexia runs deeper than a sudden distaste for food. “If you pump nutrients into them with an IV, they should get better but they don’t,” says Flint. “They keep losing weight. That’s a total mystery.”

The researchers began to wonder: “Does the tumor do something to set up the metabolic failure?” says study co-author and medical oncologist Tobias Janowitz.

To find answers, cancer researchers from University of Cambridge turned to lab mice. Some of the mice carried colorectal tumors; others had pancreatic cancer. Both cancer types often result in cachexia for human patients.

As expected, the mice developed tumors and eventually cachexia. Mice with cachexia symptoms had lower blood glucose and higher levels of stress hormones than their healthy siblings.

The cachectic mice were also having trouble breaking down fat cells and turning them into molecules called ketones, which fuel the brain during times of starvation.“The ketones are the sort-of safety circuit during periods of low food intake,” explains Janowitz.

When the scientists tested to see if the tumors were secreting chemicals that might be changing the mice’s metabolism, one immune-signalling molecule fit the bill. Its name is IL-6.

Just adding IL-6 to the bloodstreams of mice that don’t have cancer was enough to shut down their typical metabolism. Like the cachexic mice, their livers stopped making ketones.

”What we do know is that when we do our IL-6 infusion, we can induce the liver phenotype in 48 hours in mice,” says Flint. “The question is: what is the longterm consequence of an altered liver metabolism?”

For cancer patients, the consequences aren’t good. Shutting down ketone production causes the body to start burning through its own tissues. Hence the muscle and fat loss associated with cachexia.

Another effect of the metabolism shut-down is a suppressed immune response. Since the immune system finds and destroys the vast majority of tumors in early stages, secreting IL-6 may be one way that tumors protect themselves.

“It’s sort of a hijack mechanism,” explains Janowitz. Shutting down the immune system may be one way the body prevents collateral damage during infections, the researchers say. However, against cancer, the immune shut down backfires, allowing the cancer to spread.

Findings like these don’t have immediate impact in hospitals, but immune therapy is already one of the existing lines of attack against cachexia. IL-6 is a well-studied molecule, and researchers already know how to target it. It may be possible to combine immunotherapy and nutrition therapy in a way that counters cachexia, says Janowitz.

“What we’ve done for the first time in our study is that the body’s response to tumors seems to be determined to some extent by the host’s metabolic state,” says Flint. “And no one’s really appreciated. that before”

]]>http://dianacrowscience.com/cachexia-cancer-kills-metabolism/feed/28357 Things To Know About Mitochondria: 2016 editionhttp://dianacrowscience.com/7-mitochondria-2016-edition/
http://dianacrowscience.com/7-mitochondria-2016-edition/#commentsFri, 18 Nov 2016 01:50:06 +0000http://dianacrowscience.com/?p=756Mitochondria: To most people, they’re little more than a ghostly memory fragment from middle school biology. However, these tiny “powerhouse(s) of the cell” are much more than they seem.

They’re actually the shape-shifting descendants of ancient bacteria that were eaten by a larger archaebacterium billions of years ago. . (If you want to know more about that theory, check out my recent Lateral magazine piece on the scientist who developed that theory.) Mitochondria have complex relationships with other organelles, swim around in our neurons, and make up 1/3rd of the mass of heart cells. In the past year, scientists have learned how to add and remove them with cellular surgeries and how to manipulate them directly.

Mitochondria live in every cell in your body and are essential for human life. As University of California post doc Samantha Lewis pointed out to me: “There’s mitochondrial involvement in almost every disease.”

Yet, we rarely hear of or think about our cells’ powerhouses.

Here are seven facts you probably haven’t heard about mitochondria:

1: Mitochondria are interconnected shape-shifters.

We say “Mitochondria is the powerhouse of the cell” as if mitochondria is a singular word, but actually it’s plural. (The singular of mitochondria is mitochondrion.) However, in most cells mitochondria act as a collective, passing electrons and genetic information from mitochondrion to mitochondrion.

“They’re [descended from] bacteria that divide in a binary fashion,” explained UC Davis cell biologist and mitochondria specialist Jodi Nunnari. “During the course of evolution [the mitochondrial] genome has been greatly reduced. As a consequence of that and the fact that they were reproducing in a new environment, a few of those do mitochondrial fusion.” Mitochondria’s habit of merging sets them apart from all known bacteria. “Bacteria divide, but they don’t fuse,” Nunnari added.

In fact, mitochondria are so tightly connected that many scientists think of them as a membrane network rather than a series of jelly-bean shaped organelles.

2: Scientists have recently learned how to kinda control their shape-shifting.

Until recently, mitochondrial motives for fusing and dividing have remained murky. However, one team of scientists at Washington University at St. Louis have discovered one molecule that exerts an outsize influence on mitochondrial fusion.

“They have kind of a mob mentality,” Gerald Dorn, a cardiologist from Washington University in St. Louis said of mitochondria. “They do a lot of things that are out of our control.”

However, Dorn and his team recently identified a peptide that is mounted on the ends of individual mitochondria, which opens and closes “like a diaper pin”.

When the diaper pin peptide is “open”, mitochondria stick to each other like Velcro and fuse. When the diaper pin peptide is closed, the mitochondria go on their solitary way.

By adding drugs that open or close the peptide, Dorn and his colleagues were able to mostly control the rate of mitochondrial fusion in the cell. For cell biologists, that’s a new one. The study ran in the prestigious journal Nature.They’re hopeful that someday, the ability to manipulate mitochondrial merging and dividing will lead to treatments for killers like heart disease.

3: They swap genes amongst themselves.

The cell’s nucleus is a hub of genetic information, but mitochondria have kept a handful of their essential genes all to themselves.

Mitochondria store their genetic info on little globs of DNA called nucleoids, which are spread throughout the cell’s mitochondria. Although nucleoids have their own name, they can be thought of as chromosomes for mitochondria. “I do call them mitochondrial chromosomes,” Nunnari admitted.

Nucleoids get shuttled from one mitochondrial compartment to another, and only a small fraction of them are copied to make new mitochondria.

4: Mitochondria are BFFs with the Endoplasmic Reticulum.

[An artist’s rendition of a macrophage with an endoplasmic reticulum by Liz Hirst. Photo by NIMR London via Flickr & CC 2.0 license.]

Samantha Lewis, a postdoc in Nunnari’s lab, recently captured images of strategic bonding between two of cells’ oldest organelles–the powerhouse mitochondria and the molecule-delivering endoplasmic reticulum.

5: Our cells’ powerhouses have their own agenda.

Many biologists tend to forget that mitochondria have their own evolutionary goals, says Maulik Patel of Vanderbilt University. “They retain their own genes and they retain their own genetic interests, and over time, those genetic interests may not necessarily be aligned with the host’s,” he explained.

Because they’re matrilineal, harmful mutations in males don’t make much difference to a mitochondrion’s genetic legacy, Patel says. As long as the females are in good shape, the mitochondrial genome will still get passed to offspring.

“From the perspective of a mitochondrial genome, my sister is much more valuable than I am,” Patel said.

Patel’s lab found evidence of this pheonomenon in action in fruit flies, where they found a mitochondrial mutation that hurts male fertility . They published the study in eLife.

Cells have mitochondrial population control tools to stop the powerhouses from completely overrunning the cytoplasm. However, the mutant mitochondrial strain that Patel and his colleagues studied somehow dodges the population control system.

What happens next mirrors the spread of cancer cells within a body. The mutants divide and divide, overwhelming the host’s quality control mechanisms. The difference is that in this case, the drama happens between organelles within a single yeast cell.

7: We can move them with cellular surgery tools.

In May, researchers debuted a device that can cut into cell membranes with a tiny laser blade. The device burns into the cell membrane with a laser, says study co-author Michael Teitell of UCLA cuts open a small flap of the cell’s outer membrane, a puncture small enough that the cell membrane can heal itself afterwards.

The team then took their experiment a step further by injecting foreign mitochondria into the cell though a tiny glass tube.

Adding healthy mitochondria to sickly cells’ cytoplasm was enough to restore the sick cells’ overall metabolism, the team reported.

Cellular surgeries and biopsies may soon become a regular thing in cell biology. Several other groups are developing similar techniques for physically targeting and transferring microscopic cell parts.

tl;dr:

The lives of our cells’ powerhouses are more complicated than you might think.

In 2013, something strange started happening to the starfish, or sea stars, that live along North America’s Pacific Coast. Casual observers began reporting starfish that were “dissolving” or “melting”.

“What you first see is they start getting spots on them,” explains marine veterinarian Joseph “Joe” Gaydos of University of California Davis. “They [the sea stars] start shrinking, and then legs start falling off…Legs will fall off and then crawl around, so it really is like something out of a horror show.”

In 2014, researchers were able to identify a viral culprit as the immediate cause of the disintegrating sea stars, but we still know very little about how it spreads or which starfish species are most affected by it.

The dying sea stars that were easiest to spot were the ones that live close to shore. But no one knew what the mysterious Sea Star Wasting Disease (SSWD) was doing to the sea stars deep underwater and in the open ocean.

“When the sea star wasting disease hit in the Salish Sea in 2013, my first thought was, ‘Gosh, we have 29 species of sea stars. Who’s going to get hurt?’” Gaydos told me over the phone.

Luckily, the Salish Sea, an area which includes Puget Sound in Washington State and the Gulf Islands in British Columbia, Canada, is home to an organization called REEF. Since 2006, REEF has been training amateur divers to count the organisms they see, and over 8,000 of those dives have included sea star counts.

Gaydos and his colleagues, led by Diego Montecino-Latorre, analyzed the data from REEF’s dives. They also supplemented the REEF data by systematically criss-crossing the Salish Sea’s basins, counting the starfish they saw.

Sunflower Sea Stars are one of the largest sea star species in the world, as big as a car’s tire when they’re full grown, according to Gaydos.

And consistently, across five basins in the Salish Sea and along the Washington State Pacific Coast, Sunflower Sea Stars are wasting away.

“Routinely, you would see a dozen on a forty five minute dive, and now you’re seeing them on maybe six out of a hundred dives. Before 2013, you saw them on maybe 90% of the dives.” said Gaydos.

Another species–Pisaster brevispinus or the Giant Pink Sea Star– went into a sharp decline as early as 2012, prompting Gaydos and his colleagues to wonder if it might have been the first species affected by the virus. However, without more information on how the virus is transmitted and how it targets starfish, we’ll likely never know.

Meanwhile, sea urchin populations are booming, thanks to the absence of their predators and competitors. Another beneficiary of the wasting disease is the Leather Sea Star. Its population has actually grown in the Salish Sea region since 2013.

“If you’re a leather star, life is looking pretty good for you. Or if you’re a blood star,” said Gaydos.

The increase in the sea urchin population will likely mean a decrease in the amount of kelp. Gaydos says, but overall, it’s still too early to predict the longterm effects of the sea star wasting disease outbreak.

What sets this study apart from many environmental epidemiology papers is its reliance on the volunteer divers.

“Those people were doing it on their own time, of their own accord, paying for that, and their efforts have really paid off,” said Gaydos. “There’s no way we could have done this paper without all of those citizen scientists out there collecting these data.”

The 8,097 dives used in the paper were carried out by about 600 citizen divers, meaning several divers went underwater dozens of times to help count sea stars.

Thanks to their efforts, scientists now have a much clearer picture of which sea star species were most affected by the virus.

Lakes make excellent witnesses, says Utah State University assistant professor Janice Brahney. The sediment at the bottom of lakes can hold clues about life in the lake thousands of years ago, preserving everything from fossils to traces of rainfall.

“I wanted to be a detective growing up, solving puzzles and looking at trace evidence to piece together what happened,” she said. “Lakes are just really excellent recorders.”

Brahney focuses on glacial lakes, which form when giant ice sheets melt. Specifically, she’s been studying the glacial lakes high in the mountains of British Columbia. Her research could help predict how our planet will handle melting glaciers.

Most of the lakes are so remote they don’t even have names. For example, one basin has five lakes that are collectively called Coven Lakes, but the individual Coven lakes are anonymous.

However, Brahney and her colleagues access these remotes lakes through a combination of helicopters, hiking, and Google Earth gazing.

The highly detailed satellite maps contain a wealth of information including evidence of receding shorelines and melting snow and ice. Her maps are annotated with red lines that tell her where shorelines were in the late 1980s-early 1990s, alongside recent images. Although glacial melts can initially cause the lakes to grow, over time, higher temperatures cause the lakes to dry up and shrink, Brahney says.

However, lake beds contain a wealth of scientific evidence. By analyzing the chemical composition of the lake bed, scientists can tell what kind of life forms lived in the lake, what the average rainfall was thousands of years ago, and even estimate where the storms that rained on the lake came from.

Scientists track ancient storms by looking at the oxygen isotopes that are present in deeply buried lake sediment. Since different stretches of ocean have slightly different oxygen isotopes present, scientists like Brahney can estimate roughly where the storm formed. (Most storms that affect lakes in Western North America blow in from somewhere in the Pacific.)

They can also estimate when the storm happened by measuring the depth of the sediment that contains the isotopes.

Brahney and her team have also been collecting water samples from the lakes and the sediments below for chemical analysis of modern lake conditions. They’ve started to notice differences in nutrient levels as the lakes warm, but the study is still underway.

Since she moved to a town not far from The Great Salt Lake, Brahney also plans to start a research project on dust from the lake. The Great Salt Lake is the remainder of what an enormous inland sea called Lake Bonneville. At its peak, Lake Bonneville covered 19,800 square miles. It carved canyons and basins into the landscape in prehistoric Utah, Idaho, and Nevada.

Over thousands of years, Lake Bonneville shrank and become saltier and saltier. Even today, the Great Salt Lake continues to shrink, leaving large stretches of finely ground dirt exposed. Those dirt and sand particles often get picked up and blown around by the wind. However, Brahney points out, we don’t know how much of that dust is in the air Utahns breathe or what its effects are.

“Dust is an untracked component in biogeochemical cycles,” says Brahney. “We don’t have a good sense of how much material moves through the atmosphere.”

One question she intends to ask, as a biogeochemist, is: How much fertilizer and pesticide get trapped in dust? We don’t know much about the risks of inhaling fertilizer, and since people haven’t worried much about dust since the Dust Bowl in the 1920s, it’s an open-ended question.

]]>http://dianacrowscience.com/lake-beds-interview-janice-brahney-usu/feed/0749The Slow Poisoning of the UK’s Bees (and What to Do About It)http://dianacrowscience.com/slow-poisoning-uks-bees-and-it/
http://dianacrowscience.com/slow-poisoning-uks-bees-and-it/#respondMon, 19 Sep 2016 20:04:16 +0000http://dianacrowscience.com/?p=721[Photo by David Short via Flickr & Creative Commons 2.0]

“By Request” is a series of posts where I track down studies that answer questions asked by you, my blog’s readers.

High School Friend Elna asked: “Impending extinction of bees- what can prevent?”

Bees are an enormously diverse group that includes over 20,000 species, spread over 6 continents. (As far as we know, there are no bees in Antarctica.) Like other animals, bees can be vulnerable to habitat loss, changing temperatures, and pollution. However, bees do have one persistent problem that stands out: they keep getting caught in the line of fire when humans spray insecticides.

The study focuses on the main UK crop that relies on bees’ pollination is oil seed rape, aka “rapeseed“, the base ingredient of vegetable oil. In 2002, the UK government licensed a new class of pesticide called neonicotinoids for use on UK rapeseed crops.

In 2002, about 50% of the UK’s oil seed rape crops were sprayed with neonicotinoids. By 2010, that number rose to about 85%, says Woodcock. Their team analyzed data collected by citizen scientists of The Bees, Wasps, and Ants Recording Society between 1994 (several years prior to the first rounds of neonicotinoid spray) and 2012. “What we were aiming to do was a sort of Before & After study,” explained Woodcock.

Some bee species that have thrived in the UK’s neonicotinoid era, but many have not.

Crucially, the scientists’ analysis revealed that bee species that have been spotted foraging on rapeseed plants are three times more likely to have suffered population declines than bee species that don’t forage on rapeseed plants.

That result makes sense, but is a bit unnerving, given that neonicotinoids are non-lethal towards many bees, including the social hive-dwelling bees. “When the worker bees go out to forage, they can become disorientated and are less likely to make it back to the hive,” Woodcock explained. “So the effect is actually quite small, but over long time periods, it has a negative effect on the population.”

Neonicotonoids are a stark contrast to pesticides such as Naled, which kills insects instantly, Last month, several million bees were killed in South Carolina, when the county government decided to spray a mosquito-killing pesticide in order to preemptively stop the spread of Zika virus.The bee death toll was unnecessarily high, since the spray happened during the day, when bees are most likely to be out and about. If the county officials had waited until sundown, most of the bees would have been safely inside their hives or burrows, away from the deadly pesticide.

However, one of the biggest roadblocks to protecting bees is the fact that there are many species we know very little about. Social bees, with their castes of queens, drones, and workers are the best-known and most frequently studied, but they’re a minority of known bee species. The majority of bee species are solitary creatures, where one hardworking bee builds a burrow, gathers the pollen, and mothers a brood. Although solitary bees have raw numbers in their favor, most humans pay less attention to them, because they don’t produce honey. And because many bee researchers are specifically interested in hive behavior, few experiments have been conducted assessing how pesticides affect solitary bees.

Several of the UK bee species that saw a decline over the 1990s-2010s were solitary bees. It’s possible that the solitary bees also experienced disorientation that made it harder to find their way home, but the researchers really don’t know.

Woodcock urged caution before jumping to conclusions about the need to regulate or ban neonicotinoids. As detrimental as they are, they’re still probably less disastrous for bees than the pesticides that kill them instantly. “If you were to lose neonicotinoids, something else is likely to happen that would take their place, because crops like oilseed rape really do need some sort of pesticide control,” said Woodcock. “If you have to switch over to other insecticides, what will be the impacts be? And it might not necessarily just be bees; it may be contamination in the water or in the soil.”

However, bees do have one rare and potentially game-changing factor in their survival toolkit: their charisma. Many humans like bees.

(Well, as long as the bees aren’t stinging them or something…)

“One of the problems [scientist] people have always had with insect conservation is selling it to the wider community and explaining why do we need to care about these species?” said Woodcock. “One of the things that bees have done–and I never thought that it could happen–is they’ve suddenly become so important to so many people. People see bees as important for pollination and supporting crops.”

“I think part of [bees’ popularity] might be because they’re furry…” he added.

But, anyway, circling back to high school friend Elna’s original question:

Steps You Can Take to Save Bees:

Plant wildflowers in your garden. One of bees’ greatest obstacles is a loss of their natural food sources. By planting an assortment of wildflowers in a section of your garden (or a flower box, if you live in a city), you’ll feeding the local bees.

Incorporate patches of sand into your landscaping. Many bees make their burrows and nests in sand, so a strategically placed strip of sand (in a location away from the places where people walk barefoot) can help provide housing for local bees.

Vote in local elections. (And state and national ones.) A large chunk of land management decisions–such as which areas are preserved in parks, whether or not pesticides are sprayed to prevent Zika, and pollution ordinances are decided at the local level. By all means, cast your ballot for president but remember that your local government makes many decisions about what’s allowed to be sprayed.

Ease up on the pesticide use. If you’re thinking about using pesticide on your garden or lawn or flower box, stop and consider the ramifications. That’s not to say: never use any pesticide ever, but consider whether there are less lethal alternatives.

Check out (or even join) the Pollinator Partnership Project.Bees’ popularity is a major point in their favor, and the multinational nonprofit Pollinator Partnership runs projects supporting bees’ health including planting wild flowers by roadsides, helping people in cities set up flower boxes outside their windows, and running educational workshops. They’re active across most of North America.

tl;dr:

Even non-lethal insecticides can hurt bees, but the best way to help them is by planting more wildflowers for them to eat.